Abstract

Learning and memory impairment may result from age-related decline in synaptic plasticity-related proteins in the hippocampus. Therefore, exploration of functional foods capable of ameliorating memory and cognition decline is an interesting endeavor in neuroscience research. We report the effects of Anredera cordifolia (AC) extract on learning and memory deficits in a senescence-accelerated mouse-prone 8 (SAMP8) mouse model, which demonstrate age-related memory deficits and related pathological changes in the brain. After 8 weeks of oral administration of AC extract, the mice were trained in the Novel Object Recognition (NOR) task, and after 7 more weeks, in the Morris Water Maze (MWM) task. Following the completion of behavioral testing, the blood biochemistry parameters, the hippocampal levels of brain-derived neurotropic factor (BDNF), PSD95, and NR2A, and the p-cAMP-response element binding (p-CREB)/CREB ratio were measured. The AC-treated group spent more time exploring the novel objects in the NOR task, and showed faster acquisition and better retention in the MWM task than the negative control (CN) group. In addition, AC enhanced the levels of the aforementioned neuronal plasticity-related proteins, and did not affect the blood biochemistry parameters. Therefore, our data suggest that the AC extract may improve learning and memory without causing any noticeable side effects in the body.

Highlights

  • Learning and memory impairment may result from age-related decline in synaptic plasticity-related proteins in the hippocampus

  • No studies have yet been focused on the role of Anredera cordifolia (AC) extract in an age-related animal model with learning and memory impairment, or especially the effects of AC extract on synaptic plasticity-related proteins, such as the levels of brain-derived neurotropic factor (BDNF), PSD95, NR2A, and the p-cAMP-response element binding protein (CREB)/CREB ratio in the hippocampus

  • The present study suggests that Anredera cordifoila extract has potent memory-enhancing effects in senescence-accelerated mouse-prone 8 (SAMP8) mice

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Summary

Introduction

Learning and memory impairment may result from age-related decline in synaptic plasticity-related proteins in the hippocampus. SAMP8 mice represent an interesting and advantageous nontransgenic mouse model for AD research.[16] These mice exhibit phenotypes of accelerated aging,[17] including age-related impairment in learning and memory,[18] and demonstrate neuropathological changes of the synapses analogous to cognitive dysfunction in AD.[19]. Lower levels of brain-derived neurotrophic factor (BDNF)[30–32] and postsynaptic density protein 95 (PSD95)[31,33] in SAMP8 mice lead to decreased activation of CREB33 and dysfunction of NMDAR,[34] indicating that BDNF-NMDAR-PSD95-CREB-mediated synaptic plasticityrelated signaling is impaired in these mice. No studies have yet been focused on the role of AC extract in an age-related animal model with learning and memory impairment, or especially the effects of AC extract on synaptic plasticity-related proteins, such as the levels of BDNF, PSD95, NR2A, and the p-CREB/CREB ratio in the hippocampus. The purpose of the current investigation was three-fold: (i) to determine whether oral administration of AC extract affected learning and memory in the age-accelerated SAMP8 mice; if so, (ii) to elucidate the mechanisms of action of AC extract; and with regard to food safety concern, (iii) to determine whether AC extract produces any side effects in SAMP8 mice

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